Q-omics provides the consensus-scored DTL profile across patient tissues and cancer cell-line models. DTL expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, DTL is differentially expressed in 16, with the highest sampling consensus in BLCA. Additionally, DTL RNA expression shows 24,942 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, BLCA, and LSCC as cancer lineages where DTL shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for DTL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DTL survival associations across molecular data types. DTL RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DTL RNA expression–survival associations across cancer types. High DTL expression shows unfavorable associations in ACC, MESO, KIRP, LIHC, LUAD and KICH. The ACC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify ACC as the clearest survival context for DTL RNA expression.
This table summarizes DTL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for DTL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DTL shows higher tumor expression in BLCA, HNSC, KIRC, KIRP, LUAD and COAD. The BLCA box plot shows higher DTL RNA expression in tumor versus normal tissue (log2 FC = +2.596, t-test p < 0.001).
This table shows molecular features associated with DTL in patient tissues and cancer cell lines. In patient samples, DTL shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, DTL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Leukemia.
